Heart failure (HF) is a debilitating, end-stage disease in which abnormal function of the heart leads to inadequate blood flow to fulfill the needs of the body's tissues. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately fill with blood between heartbeats and the valves regulating blood flow may become leaky, allowing regurgitation or backflow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness, and inability to carry out daily tasks may result.
Not all HF patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As HF progresses, it tends to become increasingly difficult to manage. Even the compensatory responses a triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output.
Current standard treatment for HF is typically centered around medical treatment using ACE inhibitors, diuretics, and digitalis. It has also been demonstrated that aerobic exercise may improve exercise tolerance, improve quality of life, and decrease symptoms. Cardiac surgery has also been performed on a small percentage of patients with particular etiologies. Although advances in pharmacological therapy have significantly improved the survival rate and quality of life of patients, some HF patients are refractory to drug therapy, have a poor prognosis and limited exercise tolerance. In recent years cardiac pacing has emerged as an effective treatment for many patients with drug-refractory HF.
Implantable medical devices used to treat HF include, for example, pacemakers, cardiac monitors, and cardioverter-defibrillators. Such implantable devices are designed to communicate with external devices, for example, to program or reprogram the implanted devices, or to receive data from the implanted medical devices.
The wireless communication modes used in at least some known implantable devices provide less than optimal energy consumption for certain applications. Accordingly, a need exists for implantable medical devices configured to communicate with external devices via lower-power communication modes. For example, Bluetooth Low Energy (BLE) communications may be used in an implantable medical device. However, because a BLE transceiver consumes power when active, it may be desirable to place the BLE transceiver in a sleep or inactive mode until communication is necessary. In order to activate the BLE transceiver from a sleeping state, a method of sending a wakeup signal from an external programmer to the implantable medical device may be implemented. For example, U.S. patent application Ser. No. 14/969,589, filed Dec. 15, 2015 (which is incorporated by reference herein in its entirety) describes receiving a near field communications (NFC) signal from an external programmer, and using that NFC signal to activate the BLE transceiver.
However, circuitry for detecting and processing BLE communications does not typically include simple circuitry for detecting NFC signals (e.g., at 13.56 megahertz (MHz)). Instead NFC integrated circuits are often relatively complex, as they are designed to process data transmissions. Therefore, such integrated circuits consume large amounts of current.